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Laminin-8 overexpression promoted endothelial cell spreading and migration in scratch assays and accelerated angiogenic tubule formation in collagen gel overlay assays.
However, miR-200c mimic significantly reduced primary mouse and human keratinocyte migration in transwell assay (Fig. 2d), while inhibition of miR-200c in keratinocytes resulted in significant acceleration of their migration in scratch assay (Fig. 2e).
The most potent chalcones inhibited the growth of human leukemia cell lines at nanomolar concentrations, caused microtubule destabilization and mitotic arrest in human cervical cancer cells, and inhibited human breast cancer cell migration in scratch wound and Boyden chamber assays.
However, knockdown of each of these genes only led to a mild decrease in migration in scratch wounds.
Compared to SHYTG2 cell migration (~86% of migration, Figure 1Aj), we observed only 53% SHYmutant cellular migration in scratch assays when grown in similar culture conditions.
These genes included the five that most strongly inhibited migration in scratch wounds when knocked down, ARC, ZRANB1, FMNL3, FNBP3 (also known as FBP11/HYPA) and LIMD1.
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Hsp25/27, phosphorylated in response to BMP-2, localizes in actin protrusions together with BMPRII and the expression of the phosphorylation resistant mutant of Hsp27 was able to completely block migration in scratch-wound assays.
GGTI-298 also significantly reduced MCF7 cancer cell migration in scratch-wound assays (P = 0.015).
Ito et al. reported that the treatment of cultured proximal tubular cells with HMW-HA and LMW-HA resulted, through activation of MAPK signaling cascade, in increased cell migration in scratch-wound assays.
Quantification of the migration rate in scratch assay showed significantly increased migration with TGF- β2 treatment, in parallel to spheroid assay results.
Endothelial cell migration In the scratch wound assay, SV-ECs at the wound edge migrate to repopulate a denuded area created by the scratch (Fig. 2d).
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